Problems in implanted pacemakers sensing heartbeats during periods of exercise have been found to occur in patients. Exercise has been found to cause a decrease in the amplitude of cardiac signals. This finding has been confirmed by measurements of endocardial and epicardial electrograms.
In cardiac pacing, "sensitivity" is the minimum amplitude of an input signal that will cause a pacemaker to respond. A cardiac event is sensed when the amplified input signal corresponding to that event exceeds a threshold level. If the sensitivity is too low, which occurs when the amplifier gain is too low or the sensing threshold level is too high, then some cardiac events will not be sensed because even their peak signals may not exceed the threshold level. However, if the sensitivity is too high, then the high gain of the amplifier or the low threshold level may result in background noise signals causing spurious sensing of cardiac events. Generally, in prior art pacemakers, the attending physician sets the sensitivity while monitoring the amplitude of cardiac signal waveforms. The physician sets the amplifier gain so that a particular maximum cardiac signal amplitude, characteristic of a sensed heartbeat, is attained. Then the background noise level is monitored and the sensing threshold is set between the background noise amplitude and the maximum cardiac signal amplitude. The difference between the sensing threshold and the amplitude of a heartbeat signal is called the "margin".
Because cardiac signal amplitudes are reduced when a patient exercises, changes in cardiac signal amplitude due to such exercise may lead to an incorrect sensitivity setting. Various studies have shown that the respective amplitudes of cardiac electrical signals decrease during exercise. Bricker, J. T. et al., "Decrease in Canine Endocardial and Epicardial Electrogram Voltages with Exercise: Implications for Pacemaker Sensing", PACE, Vol. 11, pages 460-464 (1988), relates the results of exercise tests showing that unfiltered electrogram amplitudes are decreased in 84% of test cases. Furthermore, Frohlig, G. et al., "Atrial Sensing Performance of AV Universal Pacemakers During Exercise" PACE, Vol. 11 pages 47-60 (1988), shows that 25 of 57 (44%) dual-chamber pacemakers exhibited poor atrial sensing during exercise by the patients. Proper atrial sensing resumed in 16 of the 25 pacemakers within 1 to 7 minutes following the cessation of such exercise. In the remaining pacemakers, the atrial sensing threshold generally was decreased by one-half with normal sensing. Frohlig, G. et al., " Atrial Signal Variations and Pacemaker Malsensing During Exercise: A Study in the Time and Frequency Domain", Journal of the American College of Cardiology, Vol. 11, pages 806-813 (1988), went on to measure atrial signal variability in the time and frequency domains. Unfiltered atrial electrograms (AEGMs) from 33 patients were telemetered from an implanted pacemaker to an external monitoring computer. On the average, atrial electrocardiogram amplitudes decreased by 11% while AEGM amplitudes decreased by 11-49% in 45% of patients.
The problem of undersensing of cardiac signals during exercise is insidious for cardiac pacemaker patients who are young or athletic and whose pacemakers function in the DDD or DDDR pacing mode. In these modes (hereafter referred to as collectively as DDDX) with a normally functioning sinus node, the pacing rate is set by the rate of natural atrial heartbeats. In the DDDX pacing mode, a correctly functioning sinus node hastens the rate of atrial heartbeats in response to the onset of exercise. The DDDX pacer senses an atrial heartbeat, waits a predetermined "A-V delay" period and, unless a natural ventricular heartbeat is sensed during this period, upon the lapse of this period, delivers a pacing pulse to the ventricle. If, during exercise, the pacemaker fails to sense some or all natural atrial heartbeats (called P waves), ventricular pacing will not synchronously follow the true, natural rate of atrial heartbeats. Atrioventricular synchrony results in an augmentation of cardiac output and improved hemodynamics. [See, e.g., Levine, P. A., Mace R. C.: "Pacing Therapy: A Guide to Cardiac Pacing for Optimum Hemodynamic Benefit." Mount Kisco, N.Y., Futura Publishing Co., 1983, pp. 22-26.] It is also the only method for augmented rate increase in a DDD pacemaker.
Another hazard to a cardiac patient arises from the undersensing of atrial or ventricular cardiac signals. If a pacemaker fails to correctly sense atrial heartbeats (called P waves) or ventricular heartbeats (called R waves), the pacemaker, rather than sensing a true, i.e., natural, P or R wave and correctly inhibiting delivery of a pacing pulse to the atrium or ventricle, may erroneously deliver a pacing pulse during the repolarization of the respective chamber of the heart. Pacing during heart repolarization, particularly during the "relative refractory period" of the heart, which is known as the heart's vulnerable period, can induce an atrial or ventricular fibrillation, depending upon the chamber of origin. Ventricular fibrillation results in cardiac arrest and death without intervention. [See, e.g., Sutton R., Bourgeois I.: "The Foundations of Cardiac Pacing, Part I: An Illustrated Practical Guide To Basic Pacing." Mount Kisco, N.Y., Futura Publishing Co., 1991, p. 17.]
An additional hazard to a pacemaker patient may result from the oversensing of atrial or ventricular depolarizations. Oversensing refers to the sensing of non-atrial or non-ventricular depolarizations (e.g., electromagnetic interference, cardiac repolarization, far-field depolarization from the opposing chamber, or myopotentials). Oversensing in the atrium in a DDDX pacemaker can cause rapid ventricular pacing or the false activation of atrial upper rate behaviors. Oversensing in the ventricle can cause inhibition of ventricular output or noise reversion pacing. Ventricular inhibition could cause ventricular rates to decrease, such that the patient experiences dizziness, syncope, or cardiac standstill leading to cardiac arrest.
The operation of automatically adjusting sensitivity, by modifications to amplifier gain and to sensing threshold, has been performed in prior art pacemakers on the basis of measurements of sensed cardiac signals alone. For example, U.S. Pat. No. 4,708,144, entitled "Automatic Sensitivity Control for a Pacemaker" issued Nov. 24, 1987 to J. R. Hamilton et al., teaches an implantable pacemaker in which the sensitivity of the sense channel is automatically controlled. The peak amplitude of each R wave is measured and a long-term average is derived. The gain of the sense channel is adjusted automatically in accordance with the average of the measured peak values.
If noise voltages are present at the electrodes, then a cardiac stimulator may erroneously treat such noise as a natural heartbeat and fail to stimulate the heart when needed even though no natural heartbeat has actually occurred. Thus it is important that there be a way to discriminate between noise and a heartbeat. Noise rejection in prior art pacemakers has generally involved the making of adjustments to the pacemaker sensing threshold parameter. The "sensing threshold" is the amplitude of a sensed or input signal which is just sufficient to cause the pacemaker to recognize the respective cardiac event. By raising the sensing threshold, the effect of the noise is reduced. U.S. Pat. No. 4,779,617, entitled "Pacemaker Noise Rejection System", issued to R. H. Whigham on Oct. 25, 1988, discloses a noise rejection circuit for an implantable pacemaker. During the "relative refractory period" (RRP), as defined by the pacemaker, following a ventricular heartbeat, the pacemaker senses the peak noise amplitude. The pacemaker RRP is restarted whenever the sensed noise amplitude exceeds the previous peak noise amplitude. Following the lapse of the RRP, the peak detected amplitude, representing the noise signal, is added to the programmed threshold amplitude, and the sum thereof is used as the threshold amplitude for heartbeat sensing.
It is an object of the present invention to improve the accuracy of cardiac signal sensing when a patient is exercising.
An object of the present invention is to automatically set the sensitivity of a pacemaker as a function of a physiological sensor measurement.
An additional object of the present invention is to automatically set the sensitivity of a pacemaker as a function of both a physiological sensor measurement and the characteristics of sensed cardiac electrical signals.
It is also an object of the present invention to automatically set the sensitivity of a pacemaker as a function of a physiological sensor measurement by making adjustments to a sensing threshold parameter, an amplifier gain parameter or both parameters.
It is a further object of the invention to automatically adjust sensing sensitivity, particularly in the atrial channel, of a dual chamber pacemaker operating in a DDD mode, so that A-V synchronous pacing is provided when a patient is exercising.
A feature of the present invention is a pacemaker which automatically adjusts for the relatively lower amplitude cardiac signals which occur while a patient is exercising so that the pacemaker may employ a smaller sensing threshold safety margin than is otherwise programmable or otherwise automatically determined, based on the characteristics of the cardiac electrical signal alone, resulting in minimized oversensing of myopotentials and other electrical noise. Also, in the instance in which the sensing threshold was programmed with too small a sensing threshold safety margin, the present invention will prevent undersensing, i.e., loss of capture, of the cardiac signal during exercise.